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Patho 1 > Chap 6- Immune System > Flashcards

Chap 6- Immune System Flashcards

1
Q

What are the cell types of the immune system?

A
  • lymphocytes
  • antigen-presenting cells
  • effector cells
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2
Q

what kind of cells make up lymphocytes?

A

B and T cells

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3
Q

what are them main antigen- presenting cells?

A
  • dendritic cells

- macrophages

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4
Q

what are the main effector cells?

A
  • T lymphocytes
  • Macrophages
  • Granulocytes
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5
Q

Dendritic cells

A
  • strong antigen- presenting cells
  • expand innate response and elicit adaptive immunity
  • secrete cytokines that activate NK cells and differentiate T cells
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6
Q

What kind of cells are CD4+ cells?

A

helper T cells

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7
Q

What kind of cells are CD8+ cells?

A

Cytotoxic T cells

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8
Q

natural killer cells (NK)

A
  • kills pathogens inside the cell

- respond to IL-2 and secrete INF- gamma which activate macrophages

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9
Q

What is the main function of lymphocytes?

A

produce antibodies, neutralize pathogen, phagocytosis, complement activation

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10
Q

what is the main function of helper T cells?

A

activate macrophages, activate other T and B cells

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11
Q

what are MHC complex’s?

A
  • Major histocompatibility complex
  • proteins on antigen- presenting cells that present antigen to T cells
  • genes located on chromosome 6
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12
Q

what is human MHC proteins?

A
  • human leukocyte antigens (HLAs)

- MHC is shared throughout all mammals, HLAs are specific to humans

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13
Q

What are Class II MHC cells?

A
  • CD4+ helper T lymphocytes interact with dendritic cells and macrophages, activate CD4+ cells
  • located on antigen- presenting cells
  • is the more sophisticated class
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14
Q

What are Class I MHC cells?

A
  • present in all nucleated cells

- CD8+ activated to kill any type of virus- infected cell

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15
Q

what are the generative lymphoid organs?

A

thymus and bone marrow

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16
Q

what are the peripheral lymphoid organs?

A

lymph nodes, spleen, mucosal and cutaneous lymphoid tissues

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17
Q

lymphocyte recirculation

A
  • most important for T cells
  • T cells need to come to lymph nodes where they are activated and differentiated
  • can then go to peripheral tissues
  • B cells do not need to do this- can go anywhere
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18
Q

why are the lymph nodes important?

A

collect antigens from tissue

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19
Q

why is the spleen important?

A

captures blood- borne antigens by antigen- presenting cells in the spleen

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20
Q

what is the first line of defense?

A
  • external defense
  • physical barriers like skin, mucus, nasal hair
  • chemical barrier like oil, sweat, stomach pH
  • type of innate immunity
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21
Q

what is the second line of defense?

A
  • inflammation
  • phagocytes: macrophages and neutrophils
  • fever
  • complement system
  • NKC
  • type of innate immunity
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22
Q

What is the third line of defense?

A
  • active immunity
  • passive immunity
  • both are types of acquired immunity
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23
Q

what is active immunity?

A
  • immunity that is cell mediated (T or B cells)

- your body makes antibody when exposed to antigen

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24
Q

What is passive immunity?

A

antibody artificially produced outside is directly injected into the body

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25
Q

what happens during innate immunity?

A
  • inflammation
  • antiviral mechanisms
  • functions of epithelia
  • innate immunity is non-specific
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26
Q

What is the role of Type I IFN?

A

virus infects a cell -> cell produces type I IFN -> does not allow virus to make protein/ degrades genetic material -> virus dies

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27
Q

What are the functions of epithelia in innate immunity?

A
  • physical barrier to infection- most pathogens cannot pass
  • kill microbes by locally producing antibiotics
  • kill microbes and infected cells by intraepithelial lymphocytes (limited specificity)
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28
Q

what is defensin?

A

a type of antibiotic made by the epithelium

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29
Q

what happens during adaptive immunity?

A
  • humoral immunity

- cellular immunity

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30
Q

what is humoral immunity mediated by?

A

B cells and antibodies

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31
Q

what is cellular immunity mediated by?

A

T cells

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32
Q

what is the innate immunity mechanism?

A
  • ready to react to pathogens
  • not specific to any particular pathogen
  • works in first 6-12 hours of infection
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33
Q

what is the adaptive immunity mechanism?

A
  • stimulated by microbes and non-microbial substances
  • works within 1-5 days after infection
  • results in very specific responses
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34
Q

innate immunity receptors

A
  • recognize PAMPs and DAMPs
  • can respond to any type of microbe
  • receptors are not diverse
  • receptors are non- clonal
  • innate immunity does not harm healthy cell
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35
Q

adaptive immunity receptors

A
  • have different microbes with specific receptors for each
  • many different receptors due to genetic changes
  • receptors are specific to an antigen
  • more likely to cause autoimmune diseases
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36
Q

how does the binding of an antibody inactivate antigens?

A
  • neutralization- bind to important parts of microbe so it cannot be recognized by receptor, more easily phagocytized
  • agglutination- glue microbes together so easier to phagocytize
  • precipitation of antigen- form long chain and precipitate out of solution to be more easily phagocytized
  • activate complement system
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37
Q

how do naive B cells become mature?

A
  • naive B cells have not encountered any pathogens
  • produce IgM
  • once B cells introduced to microbe with help of helper T cells, start to proliferate/differentiate
  • can differentiate into different classes of immunogloblulins
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38
Q

Ig Class switching

A
  • B cells go through class switching with the help of helper T cells
  • IgM -> IgG, IgE or IgA depending on situation
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39
Q

IgM

A

complement activation

40
Q

IgG

A
  • neonatal immunity

- passes through placenta to fetus

41
Q

IgE

A
  • allergic reaction
  • Helminths
  • found on mast cells who produce histamines
42
Q

IgA

A

antibody in mucus, tears, saliva

43
Q

affinity maturation

A
  • want B cells anitibodies to have a very high affinity for anitgen
  • subgrouped into T depended and T independent
44
Q

T- dependent affinity maturation

A
  • helper T cells help B cells to do class switching
  • have high affinity for antibodies
  • long-lived
45
Q

T- independent affinity maturation

A
  • results in IgM
  • low affinity antibodies
  • short- lived
46
Q

primary antibody response

A
  • 5- 10 day lag time
  • peak response is small
  • usually produces IgM to IgG
  • Lower affinty
47
Q

Secondary antibody response

A
  • repeated infection
  • 1-3 day lag time
  • large peak response
  • increase in IgG, in some situations can have class switching as well (higher affinity)
48
Q

migration of T cells

A
  • naive T cells migrate from blood into lymph nodes
  • in lymph nodes T cells activated by antigens
  • Activated T cells leave nodes, enter blood stream, migrate to peripheral tissues
49
Q

acute viral infections

A
  • CD8+ T cells proliferate and differentiate into effector cytotoxic T cell and memory cells
  • clear virus
50
Q

chronic viral infection

A
  • CD8+ cells initially respond
  • there is a response, but does not last as long because inhibitory receptors are expressed
  • virus is able to persist
51
Q

what is hypersensitivity?

A
  • excessive, uncontrolled or misdirected immunological reaction
  • occurs in allergic reactions or autoimmune diseases
52
Q

what triggers hypersensitivity?

A

exogenous or endogenous antigens

53
Q

atopy

A

increased susceptibility to develop hypersensitivity reaction

54
Q

atopy

A

increased susceptibility to develop hypersensitivity reaction

55
Q

Hypersensitivity Type I

A
  • allergen introduced
  • Helper T cells activated, stimulate B cells to make IgE
  • IgE binds to receptor on mast cell -> sensitized
  • activated mast cell secretes vasoamines and lipid mediators (histamine and serotonin) , cytokines
56
Q

what is the immediate response to hypersensitivity I?

A
  • release of histamine and serotonin
  • vasodilation
  • vascular leakage
  • smooth muscle spasm
  • caused by prostaglandins and leukotriens, histamines, proteases
57
Q

clinical examples of type I hypersensitivity

A
  • allergic rhinitis
  • food allergy
  • bronchial asthma
  • anaphylaxis
58
Q

what is the late phase reaction of hypersensitivity I reactions?

A
  • leukocyte infiltration
  • epithelial damage
  • bronchospasm
  • caused by cytokines and chemokines
  • occures 2-24 hours after
59
Q

what is a hypersensitivity type II reaction?

A
  • antibody mediated diseases- anything except IgE

- can be caused by opsonization and phagocytosis, complement system, or antibody- mediated cellular dysfunction

60
Q

What is a hypersensitivity type III reaction?

A
  • antigen- antibody complex is formed
  • antigen- antibody complex deposited in various tissues
  • immune complex- mediated inflammation and tissue injury occurs i.e. fever, joint pain, lymph node enlargement
61
Q

clinical examples of type III hypersensitivity reactions

A
  • systemic lupus erythematosus

- reactive arthritis

62
Q

What is a hypersensitivity type IV reaction?

A
  • has nothing to do with B cells or antibodies
  • mediated by T cells
  • CD4+ mediated inflammation: delayed, secrete cytokines that stimulate inflammation and activate phaygocytes, inflammation and tissue injury occurs
  • CD8+ directly kill cells by perforins and granzymes
63
Q

perforins

A

enzyme inside T cell, produces pores

64
Q

granzymes

A

lysing enzyme

65
Q

clinical examples of hypersensitivity type IV reactions

A
  • type 1 diabetes
  • contact sensitivity
  • Tb
66
Q

autoimmune disease

A
  • loss of self-tolerance
  • involves both T and B cell responses
  • body naturally produces reactive b and t cells that are reactive, body has tolerance to these reactive cells in healthy people
67
Q

are autoimmune diseases seen more often in men or women?

A

women

68
Q

what is central tolerance?

A
  • occurs in thymus and bone marrow

- reactive lymphocytes go through apoptosis, receptor editing, or dev of regulatory T lymphocytes

69
Q

what is receptor editing?

A

b cells change their receptor specificity through genetic modifications

70
Q

peripheral tolerance

A
  • regulatory t lymphocytes surpress reactive t or b lymphocytes
  • anergy occurs
71
Q

what is anergy?

A
  • occurs in peripheral tissues

- lymphocyte recognizes antigens but are functionally unresponsive due to lack of co-stimulating signals

72
Q

what do costimulators do?

A

cause self tolerance failure on antigen presenting cells

73
Q

what is molecular mimicry?

A
  • occurs in T and B cells
  • T cells recognize microbial agent which is similar to self antigen
  • results in cross reaction and T cells are activated
  • Tissue is damaged
74
Q

systemic lupus erythematosus

A
  • autoimmune diseases
  • blood serum has autoantibodies, especially antinuclear antibodies (ANA)
  • Anti-Sm is specific type of autoantibody associated with SLE
  • cause is deposition of immune complexes and binding of anitbodies to cells and tissues
75
Q

SLE Etiology

A
  • genetic factors
  • defective elimination of self reactive B cells
  • ineffective peripheral tolerance mechanism
  • UV light inducing apoptosis, promotes inflammation
76
Q

clinical manifestations of SLE

A
  • usually young woman
  • butterfly rash!!
  • hematologic symptoms
  • arthritis
  • fever
  • fatigue
77
Q

graft

A

healthy tissue taken from one part of the body to replace diseased or injured tissue removed from another part of the body

78
Q

autograft

A

transfer of tissue from one location of persons body to another

79
Q

isograft

A

transplantation between two genetically identical individuals (twins)

80
Q

allograft

A
  • aka homograft
  • transplant of organ or tissue that comes from another person of same species
  • most common type of graft
81
Q

xenograft

A

transfer of tissue or organ between members of different species

82
Q

alloantigen

A
  • antigen of allograft and main target of rejection

- proteins encoded by MHC

83
Q

allorecognition

A
  • donor antigen presenting cells present graft via MHC II to patient T cells
  • recipient antigen presenting cell uptake alloantigen, present it to its own T or B cells
84
Q

transplant sensitization

A
  • graft antigens expressed on donor dendritic cells transported to peripheral lymphoid organs
  • alloantigen specific T cells activated
85
Q

Transplant Rejection

A
  • T cells migrate back into graft and destroy graft cells

- cytokines are produced against graft antigen

86
Q

mechanisms of graft rejection

A
  • hyperactive rejection
  • acute rejection
  • chronic rejection
87
Q

hyperactive rejection

A
  • circulating alloantigen binds to surface of endothelial cell
  • complement sys activated, inflammation, and thrombosis
  • occurs almost immediately after transplant
88
Q

acute rejection

A
  • months after transplant

- cytotoxic T cells react with endothelial cells, cause inflammation aka endothelialitis

89
Q

chronic rejection

A
  • years after rejection
  • occurs if patient stops immunosuppressive therapies
  • progressive issue that is normally controlled through immunosuppressives
  • causes fibrosis and vessel occlusion (graft arteriosclerosis)
90
Q

primary immunodeficiency

A
  • hereditary
  • manifests between 6 mo to 2 years
  • can be innate or adaptive deficiency
91
Q

secondary immunodeficiency

A
  • due to infections, malnutrition, aging, immunosuppression, autoimmunity, and irradiation/chemotherapy
92
Q

HIV/ AIDS

A
  • HIV-1 main cause in US
  • virus contains RNA
  • enzyme has reverse transcriptase that makes DNA from RNA
  • most drugs target reverse transcriptase
93
Q

HIV transmission

A
  • sexual contact
  • IV drug use
  • vertical transmission (mother -> child)
94
Q

stage 1 of HIV infection

A
  • acute stage
  • 2-4 weeks after infection
  • flu like symptoms
95
Q

Stage 2 of HIV infection

A
  • clinical latency
  • HIV has low low level of virus production- doesnt proliferate at high level
  • chronic HIV infection may take years
  • CD4 cell counts decrease
96
Q

stage 3 of HIV infection

A
  • AIDS
  • almost no CD4
  • virus levels very high
  • daignosis based on CD4 count

Patho 1 (12 decks)

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